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1.内蒙古医科大学中医学院,呼和浩特 010010
2.内蒙古医科大学医学模拟中心,呼和浩特 010010
3.内蒙古医科大学实验室与实验设备管理中心,呼和浩特 010010
博士研究生。研究方向:中医药治疗糖尿病溃疡及作用机制。E-mail:luchang199812@163.com
主任医师,教授,博士生导师。研究方向:中医药治疗糖尿病溃疡机制。E-mail:sjp4321@126.com
收稿:2025-11-09,
修回:2026-03-28,
录用:2026-03-30,
纸质出版:2026-04-30
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陆畅,党赢,王璐,等.中药调控氧化应激促进糖尿病创面愈合的机制研究进展 [J].中国药房,2026,37(08):1080-1084.
LU Chang,DANG Ying,WANG Lu,et al.Research progress on the mechanism of traditional Chinese medicine regulating oxidative stress to promote diabetic wound healing[J].ZHONGGUO YAOFANG,2026,37(08):1080-1084.
陆畅,党赢,王璐,等.中药调控氧化应激促进糖尿病创面愈合的机制研究进展 [J].中国药房,2026,37(08):1080-1084. DOI: 10.6039/j.issn.1001-0408.2026.08.19.
LU Chang,DANG Ying,WANG Lu,et al.Research progress on the mechanism of traditional Chinese medicine regulating oxidative stress to promote diabetic wound healing[J].ZHONGGUO YAOFANG,2026,37(08):1080-1084. DOI: 10.6039/j.issn.1001-0408.2026.08.19.
糖尿病创面愈合进程复杂,其难愈性与机体持续氧化应激状态紧密相关。中药通过多靶点、多通路调控氧化应激反应,在推动糖尿病创面修复中展现出独特优势。本文综述了中药调控氧化应激促进糖尿病创面愈合的机制,发现中药单体(芦丁、黄芩苷、忍冬苷、姜黄素等)、提取物(白子菜水提物、黄精提取物、银杏叶提取物等)以及复方(拔毒生肌散、当归四逆汤、复方ANBP等)可通过介导氧化应激相关通路(如核因子红细胞2相关因子2、核因子κB、糖基化终产物/糖基化终产物受体、沉默信息调节因子1等),有效缓解糖尿病创面氧化应激损伤,其机制主要体现在:激活抗氧化防御系统、抑制炎症反应、改善线粒体功能,从而协同促进创面愈合。
The process of diabetic wound healing is highly complex, and the persistence of non-healing wounds is closely associated with sustained oxidative stress in the body
. Traditional Chinese medicine (TCM) demonstrates unique therapeutic advantages in promoting diabetic wound repair by modulating oxidative stress through multiple targets and pathways. This article presents a systematic review of the mechanism of TCM regulating oxidative stress to promote diabetic wound healing. It has been found that TCM monomers (such as rutin, baicalin, lonicerin, and curcumin), extracts (including aqueous extract of
Gynura divaricata
, extract of
Polygonatum kingianum
, extract of
Ginkgo biloba
leaves, etc), and compound formulations (such as Badu shengji powder, Danggui sini decoction, Compound ANBP, etc) can effectively alleviate oxidative stress-induced damage in diabetic wounds by modulating related signaling pathways, including nuclear factor-erythroid 2-related factor 2, nuclear factor κB,advanced glycation end products (AGEs)/receptors of AGEs, and silencing information regulatory factor 1. The underlying mechanisms are mainly manifested as: activating the antioxidant defense system, inhibiting inflammatory response, and improving mitochondrial function, thereby synergistically promoting wound healing.
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